4.7 Review

Metabolic Homeostasis of Amino Acids and Diabetic Kidney Disease

Journal

NUTRIENTS
Volume 15, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/nu15010184

Keywords

amino acids; metabolic homeostasis; metabolites; diabetic kidney disease; intestinal microecology

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Diabetic kidney disease (DKD) affects a significant percentage of diabetic patients and poses a high risk of kidney failure. Current treatments focusing on glucose lowering and blood pressure control have shown no beneficial impact on preventing progression to kidney failure. This review explores the relationship between kidney dysfunction and the metabolic homeostasis of specific amino acids, and highlights the regulation effects of certain metabolites on DKD progression. The paper suggests an optimized protein diet strategy to manage amino acid homeostasis and reduce the risks of DKD in hyperglycemic conditions.
Diabetic kidney disease (DKD) occurs in 25-40% of patients with diabetes. Individuals with DKD are at a significant risk of progression to end-stage kidney disease morbidity and mortality. At present, although renal function-decline can be retarded by intensive glucose lowering and strict blood pressure control, these current treatments have shown no beneficial impact on preventing progression to kidney failure. Recently, in addition to control of blood sugar and pressure, a dietary approach has been recommended for management of DKD. Amino acids (AAs) are both biomarkers and causal factors of DKD progression. AA homeostasis contributes to renal hemodynamic response and glomerular hyperfiltration alteration in diabetic patients. This review discusses the links between progressive kidney dysfunction and the metabolic homeostasis of histidine, tryptophan, methionine, glutamine, tyrosine, and branched-chain AAs. In addition, we emphasize the regulation effects of special metabolites on DKD progression, with a focus on causality and potential mechanisms. This paper may offer an optimized protein diet strategy with concomitant management of AA homeostasis to reduce the risks of DKD in a setting of hyperglycemia.

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